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ARS Home » Plains Area » Fargo, North Dakota » Edward T. Schafer Agricultural Research Center » Sugarbeet and Potato Research » Research » Publications at this Location » Publication #301176

Title: First report of QoI-insensitive powdery mildew (Erysiphe polygoni) on sugarbeet in the United States

Author
item Bolton, Melvin
item NEHER, OLIVER - Amalgamated Sugar Company

Submitted to: Plant Disease
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/17/2014
Publication Date: 7/1/2014
Citation: Bolton, M.D., Neher, O.T. 2014. First report of QoI-insensitive powdery mildew (Erysiphe polygoni) on sugarbeet in the United States. Plant Disease. 98(7):1004.

Interpretive Summary: Sugarbeet powdery mildew is caused by the fungus Erysiphe polygoni and occurs principally in sugarbeet growing regions in western United States. In these regions, the quinone outside inhibitor (QOI) fungicides pyraclostrobin and trifloxystrobin have been important tools to manage powdery mildew. However, researchers in Idaho reported poor disease control despite QOI application starting in 2011. In 2013, a research plot near Parma, ID containing natural powdery mildew infection received treatments of pyraclostrobin, trifloxystrobin, or was untreated (control). However, plants that received either QOI treatment had similar disease levels to plants that received no fungicide application, suggesting that plants were diseased from a QOI-resistant population of E. polygoni. To gain insight into the molecular basis of fungicide resistance in this fungus, we initiated experiments to clone the E. polygoni cytochrome b gene, which encodes the protein that is targeted by QOI fungicides. We then sequenced the gene from samples taken from QOI-treated plots and control plots. Without exception, all QOI-treated samples harbored a mutation that encoded a G143A mutation. This is the first report of QOI resistance and the associated cytochrome b G143A mutation in E. polygoni. The G143A mutation has been reported in most QOI-resistant pathogens to date. When the G143A mutation dominates in a pathogen population, there is a consistent association with a loss of disease control despite QOI application. Careful monitoring and judicious use of QOI fungicides will be necessary to ensure QOI fungicides remain efficacious for powdery mildew management in the United States.

Technical Abstract: The $2.1 billion United States sugar beet (Beta vulgaris L.) industry is the primary provider of domestic sucrose. Sugar beet powdery mildew is caused by Erysiphe polygoni DC and occurs principally in sugar beet growing regions in western United States. In these regions, the quinone outside inhibitor (QOI) fungicides pyraclostrobin (Headline, BASF, NC) and trifloxystrobin (Gem, Bayer Crop Science, NC) have been important tools to manage powdery mildew since registration in 2002 and 2005, respectively. However, researchers in Idaho reported poor disease management despite QOI application starting in 2011. In 2013, a research plot near Parma, ID containing natural powdery mildew infection received treatments of pyraclostrobin, trifloxystrobin, or was untreated (control). Since there was no significant reduction in disease levels between QOI-treated blocks and untreated control blocks, experiments were conducted to clone a partial fragment of the E. polygoni cytochrome b (cytb) gene to gain insight into the molecular basis of QOI resistance in this pathosystem. The primers MDB-920 (5’-CACATCGGAAGAGGTTTATA-3’) and MDB-922 (5’-GGTATAGATCTTAATATAGCATAG-3’) were designed based on consensus sequences of several fungal cytb genes obtained from GenBank (data not presented) and used to amplify a 575-bp fragment of the E. polygoni cytb gene using DNA isolated from 12 infected leaf samples collected in September 2013 from the Parma research plot. Each sample consisted of three leaves harvested from three plants (one leaf per plant) in an experimental block. All DNA extraction, PCR, and sequencing procedures were as described previously (1). PCR products derived from six QOI-treated samples and six untreated samples were sequenced directly. Without exception, all QOI-treated samples harbored a point mutation at nucleotide position 143 that encoded a G143A mutation compared with cytb sequence from untreated samples. The two identified cytb haplotypes have been deposited in GenBank under accession numbers KF925325 and KF925326. This is the first report of QOI resistance and the associated cytb G143A mutation in E. polygoni. The G143A mutation has been reported in most QOI-resistant pathogens to date (2). When the G143A mutation dominates in a pathogen population, there is a consistent association with a loss of disease management despite QOI application (3). Careful monitoring and judicious use of QOI fungicides will be necessary to ensure QOI fungicides remain efficacious for sugar beet powdery mildew management in the U.S.